NETosis (Neutrophil Extracellular Traps) is a mode of neutrophil cell death involving decondensation of chromatin and its merging with cytoplasmic granule proteins to create a net-like structure for entrapping pathogenic elements. Patients with chronic granulomatous disease (CGD) are unable to produce sufficient NETS and are therefore immune deficient. Furthermore excessive NETs contribute to complications in many inflammatory conditions such as sepsis, lupus, cancer, acute respiratory distress syndrome (ARDS) and deep vein thrombosis. NETosis proceeds by one of two major mechanisms: ROS-dependent and ROS-independent. The ROS-dependent pathway involves the activation of protein kinase C (PKC) followed by ROS production by NADPH oxidase whereas the ROS-independent one involves activation of the Ca+2-dependent enzyme PAD4.
Although extensively researched, a standardized method for a high throughput quantitative assessment of NETosis is not available despite the great need for it in view of the rapid proliferation of biological and chemical agents exhibiting poorly characterized potentials to induce NETosis and diseases that involve NETosis.